Effect of mineral dusts on metabolic cooperation between Chinese hamster V79 cells in vitro.

Abstract

The mode of action of inorganic fibers as carcinogens is unknown. There is conflicting evidence whether they act by inducing lesions in DNA, such as initiating carcinogens, or alternatively act as promoters of carcinogenesis. Recent evidence has suggested that promoters inhibit the process of cell-to-cell chemical communication known as metabolic cooperation. Chinese hamster V79-4 cells in culture exhibit metabolic cooperation which can be blocked by the promoter tetraphorbol-13-acetate (TPA). Three kinds of mineral dust were tested to determine whether or not they could interfere with the intercellular communication. The three dusts studied were: amosite, a fibrous asbestos from the Union Internationale Contre le Cancer (UICC) standard reference series, which is a typical carcinogenic fibrous dust inducing pleural tumors following intrapleural injection into rats; ball-milled amosite, a nonfibrous dust derived from UICC amosite by ball-milling, which has the physical properties characteristic of a noncarcinogenic dust; and Min-U-Sil silica, a widely available sample of fibrogenic quartz which does not induce pleural tumors following intrapleural injection into rats. The results demonstrated that metabolic cooperation between V79-4 cells cannot be reduced by carcinogenic asbestos fibers or by relatively large numbers of nontoxic dust particles. It is concluded that if inorganic fibers promote carcinogenesis, then they do not operate by blocking metabolic cooperation.